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Cytokines and growth factors transduce their signals following ligand/receptor engagement through sequential protein/protein and protein/DNA interactions. It appears that one mechanism utilized by growth factors to modulate these processes is through protein phosphorylation/dephosphorylation. In addition, there is now compelling and extensive literature indicating that growth factors may activate distinct and/or overlapping signaling cascades that ultimately control cellular activity. Several issues in the filed of signal transduction remain elusive. How do different signaling pathways elicited by one ligand converge to regulate cell type-specific function? How do different growth factors combine to regulate cellular activity? as well, how do modifications in these signaling processes lead to disease such as cancer. My research project focus on addressing these questions to understand signaling mechanisms elicited by the cytokine/hormone prolactin leading to cell proliferation, differentiation survival and carcinogenesis.
Prolactin (PRL) is a member of the class I cytokine family of growth factors that include in addition to PRL most of the interleukins, interferon (IFN) a / b, erythropoietin, granulocyte colony-stimulating factor, leukemia inhibitory factor, oncostatin M, ciliary neurotrophic factor, as well as growth hormone. These factors play critical role in regulating cellular homeostasis of different cell types. The PRL receptor (PRLR) is also a member of the class I cytokine receptor family. Ligand binding to the PRLR induces receptor dimerization and activation of a novel signaling cascade designated as the Janus tyrosine kinase (Jak)/signal transducer and activator of transcription (Stat) signaling pathway. This intracellular pathway transmits signals for many cytokines and growth factors to target genes in the nucleus. In addition to the fundamental role of the Jak/Stat pathway in normal cell signaling, accumulating evidence is defining a critical role for this pathway in oncogenesis. Current evidence indicates that one mechanism by which the Jak/Stat contributes to oncogenesis involves prevention of apoptosis, thereby conferring a survival advantage and, potentially, resistance to chemotherapy. Moreover, the Jak/Stat pathway is known to be a target for many viral and cellular oncoproteins. My research projects involve the characterization of the Jak/Stat pathway downstream of the PRLR leading to mammary epithelial cell differentiation, survival and carcinogenesis. We are currently, examining mechanisms and signaling pathways that may positively or negatively modulate signal transduction through the Jak/Stat pathway.